case 5 Flashcards
GAD
6 months of persistent anxiety without cause. anxiety about a wide range of issues rather than a specific event like phobia, free floating not linked to a cause. more common in females. 1/20, 20yr. projections from amygdala to PAG and diffuse modulatory result in anxiety, projections to hypothalamus maintain state of anxiety. hippocampus inhibits CRH release, can become saturated and die, benzodiazepines/SSRIs first line treatment
signs and symptoms
psychological symptoms-worry, dread, poor conc, irritability
physical symptoms-trembling, nausea, shortness breath, headaches, irritability, sleep, restless.
behavioural symptoms-putting things off, avoidance, drug taking. 6/12 in ICD10. last longer than 6 months.
aphasia
inability to speak write or understand spoken or written work from a lesion to brain. sensory, motor, conductive, global.
wernikes
found in superior temporal gyrus identify and comprehend words that are performed.
circuit for spoken language
- When a person hears a sentence, this is transmitted via the auditory apparatus to the primary auditory cortex in the temporal lobe.
- This then connects to Wernicke’s area, which decodes the language into meaning.
- If the sentence is to be repeated, or replied to, the information has to be transmitted forwards to Broca’s area (expressive speech) in the frontal lobe (via the arcuate fasciculus).
- Broca’s area then produces speech via the motor programmes of the motor cortex, which activate the tongue and laryngeal muscles.
circuit for understanding written language
- Visual input is transmitted to the visual cortex in the occipital lobe.
- Input from the visual association area is sent to the left angular gyrus, where the objects are recognized and named.
- Input then goes to Wernicke’s area, where words are assembled into sentences, and the appropriate messages are sent via the arcuate and superior longitudinal fasciculi to Broca’s area.
test for CN I
olfactory. occlude one nostril, different smells. eyes closed. ask strength of smell.
CN II
optic. snellen chart one eye at a time-visual acuity. visual fields, look at me, cover one eye, say now when can see. 8 times per eye. Opthalmoscope-Optic disc, fovea, pupil reactions rate of reflex, look ahead. into distance then at finger. accomodation.
CN III
occulomotor. pupillary light reflex. H test up down and medially. ask if double vision. hold head.
CN IV
trochlear, superior oblique, H test down and medial.
CN V
trigeminal. muscles mastication-masseter whilst bite, open against resistence, temporalis whilst bite, side to side against resistence. sensation of face sharp or dull. first on clavicle. corneal reflex
CN VI
abducens-lateral rectus H test laterally
CN VII
facial. raise eyebrows, blow cheecks, prize lips or eyes open taste ant 2/3.
CN VIII
vestibulocochlear- rienne and weber test. distract one ear whilst say something in other. hearing machine for frequencies heard.
CN IX
glossopharyngeal-gag, taste post1/3 say aahh inspect palate
CN X
vagus-swallow, speak, say aahh,
CN XI
accessory-raise trapezius and SCM
CN XII
hypoglossal-stick out tongue move side to side. see if twitch.
recovery after brain injury
.axonal sprouting-formation new connections in cortex. Neurogenesis-formation new neurons. Angiogenesis-new blood vessels. Growth factor regulation such as FGFs and EPO to promote erecovery. Oligodendrocyte precurser cells. hypoexcitability.
neuroplasticity
cellular changes and cortical remapping. ability to learn and modify. strongest in childhood. children recover from stroke better as brains still developing plastic state make circuit connections needed to repair. synaptic pruning-weaker connections are eliminated whilst stronger ones are strengthened.
lower motor neurons
those that innervate the arms are in the cervical enlargement those that innervate the leg aer in the lumbar enlargment. spinal cord segments that innervate a large amount of muscles have a swollen ventral horn. Directly innervated by local circuit in SC or CS, or indirectly in higher centres. Y fibres regulate sensory input to set intrafusal muscle fibre length.
damage is loss of reflex, paralysis, loss muscle tone, atrophy, fibrillations.
lateral spinothalamic tract
pain and temperature. nerve cell body of 1st order neurons in dorsal root ganglion. terminate in dorsal horn. deccusate, ascend in contralateral lateral spinothalamic tract, pass through spinal lemniscus and terminate in VP nucleus of thalamus. Third order neurons project to somatosensory cortex.
ventral spinothalamic tract
crude touch and pressure. NCB in dorsal root ganglion. terminate in dorsal horn. asend segments before decussating then ascend in contralateral spinothalamic tract, pass in spinal lemniscuc and terminate in VP nucleus of thalamus. Third order neurons to somatosensory cortex.
dorsal columns
proprioception, discriminative touch and vibration. gracilis from lower limb. cell bodies in dorsal root ganglion, ascend in ipsilateral sorsal column to the medulla. axons in fasciculus gracilis terminate in cucleus gracilis etc. second order neurons deccusate and ascend in medial lemniscus terminate in VP of thalamus. third order neurons project to somatosensory cortex.
ascending pathways of the head-trigeminothalamic pathway
first order neurons synapse in trigeminal nucleus-mesencephalic propriception. chief touch and pressure. spinal pain and temperature. facial glossopharyngeal and vagus nerve also convey some general sens info from head and neck. second order neurons deccusate and ascend in contralateral trigeminothalamic tract, terminate in VP nucleus of thalamus. third order go to somatosensory cortex of postcentral gyrus. parietal lobe.
corticospinal/pyramidal tract
cell bodies of UMN are in PMC. pass through the corona radiata, through posterior limb of internal capsule, through midbrain in crus cerebri. 25-90% deccusate in medulla enter lateral corticospinal tract, remaining desend ipsilateral in ventral corticospinal tract, these decussate near termination. UMN synapse to LMN in ventral horn. LMN axons terminate in neuromusc junction
corticubulbar
precentral gyrus, corona radiata, internal capsule, superior cerebral peduncle. brainstem. synapse with motor nuclei of CN. contralateral, bilaterally innervated apart from hypoglossal and facial. facial above eye bilateral.
spinocerebellar tract
Ascending tract which carries information from muscle spindles, Golgi tendon organs and tactile receptors to the cerebellum. It is involved in the control of posture and coordination of movement.
vestibulospinal
Descending tract which originates in the vestibular nucleus. Controls extensor muscle tone and is involved in the maintenance of posture. regulates head position by reflex by activating neck muscles in responce to semicircular canals. VOR.
reticulospinal
Descending tract which originates in the reticular formation of the pons and medulla. Mediates the pressor and depressor effects of the cardiovascular system and the control of breathing.
tectospinal tracts
Descending tract which originates in the superior colliculus. Most fibres terminate in the cervical region of the spinal cord and it is thought to mediate reflex movements in response to visual stimuli.
rubrospinal tract
Descending tract which originates from the red nucleus of the midbrain. It controls the tone of limb flexor muscles. It receives afferent fibres from the motor cortex and the cerebellum.
spinoreticulothalamic
Ascending tract that arises in the spinal cord and ascends to the reticular formation. Reticulothalamic fibres ascend to the thalamus and synapse with thalamocortical fibres. It is thought to provide a route by which dull aching pain is consciously recognized.
ischaemic stroke
brain artery blocked, 80% strokes. embolic-forms outside brain. thrombotic-forms in brain.
haemorrhagic
brain artery burst. intracerebral-blood enters into substance of brain. subarachnoid-blood enters spaces surrounding brain.
occlusion in anterior cerebral artery
paralysis and sensory loss in contralateral leg.
occlusion in middle cerebral artery
most common site. contralateral paralysis in face or arm. somatosensory deficits. speech defects.
occlusion in basilar and posterior cerebral artery
coma or blindness.
spinal cord arteries
spinal and radicular arteries. occlusion, anterior cord syndrome, paraplegia.
penumbra area
surrounding region to stroke, blood S compromised cell under threat, can be rescued if treatment early.
risk factors of stroke
Asian/black. Age above 40. Male, hypertension, hypercholesterolemia, diabetes, smoking, family history, cardiac disease
stroke definition
rapid onset of cerebral deficit lasting greater then 24hr or death with no other cause than vascular
completed stroke
deficit is maximal usually in 6 hrs.
Stroke in evolution
progression in first 24hrs
Transient Ischaemic attach
sudden focal deficit lasting less than 24hrs with complete recovery. tendancy to reacur.
small vessel/lacunar infarcts
supply deep structures. like BG, thalamus, IC, brainstem. usually by hypertension.
epidemiology
second common cause death. uncommon below 40. death rate 20%
3 things that cause ischaemic damage
neurotransmitters glutamate, ions Ca and Na, free radicals abnormal O2.
lead to excitotoxicity, reperfusion injury, free radical formation, apoptosis, inflamation, periinfarct depolarisation
exocitoxicity
hypoxia leads to inadequate supply ATP, failure membrane pumps. inc release glutamate into extracellular fluid. influx Ca and Na. Ca overload causes formation of free radicals. mitochondrial injury, inc NO, protease activation, phospholipase activation, result cell death through necrosis.
reperfusion injury
restoration of BF to an ischaemic area leads to inflamation and oxidative stress which causes death of more neurons.
oxidative stress/free radical formation
FORMATION no AND SUPEROXIDE TO FORM SUPEROXYNITRATE. RESULTS IN LIPID PEROXIDATION, PROTEIN OXIDATION, dna DAMAGE
apoptosis
programmed cell death. oxidative stress causes mitochondrial injury, realeases cytochrome C which activates paracaspases into caspases. DNA damage and cell death.
inflamation
doesnt normally occur in brain, occurs due to brain damage, compromised BBB, microglia degrade extracellular matrix, neutrophils from liver can accsess BBB. outcome poor if already have inflam disease like obesity and arthritus.
purpose investigation
Distuinguish what type, look for underlying causes and direct treatment, exclude other causes.
imaging
Non contrast CT show heamorrhage. MRI shows changes due infarction. Diffusion weighted MRI can detect infarction. doppler ultrsound, carotid bruit heard in ICA stenosis. ECH to show if acrdioembolic source. look for cardiac enzymes to see if MI.
amaurosis fungax
– sudden loss of vision in one eye. This is due to an embolus in the retinal arteries.
treatment
drugs for hypertension, endarectomy, speech therapy, anticoag(warfarin/heparin) antiplatlet(aspirin/clopedigrol) tPa, heamorrhagic stroke:anticonvulsants, osmotic diuretic, antihypertensive
Long term managment
antihypertensive, anticoag, antiplatlet.
NIH assessment scale.
11 items between 0-4. 0 is normal function. conciousness, eye movement, visual field, facial palsy, motor arm, motor leg, limb ataxia, sensory, language, speech, extinction and inattention.
MRC grading muscle power
0-5 5 being normal power
watershed infarcts
affects two arteries like ACA MCA cause by occlusion ICA
saccular aneurysms
develop in circle of wilils
sub arachnoid and sub dural heamorrhage. extradural
in artery aneurysm,
in vein.
rupture middle meningeal artery. fracture temporal bone
